Promoting functional recovery to CNS or PNS injury requires maximizing neuronal survival, facilitating axon growth, remyelination and appropriate synapse formation. This last step is particularly important since formation of new synapses with inappropriate targets could produce maladaptive consequences. Tactile allodynia, characterized by hypersensitivity to innocuous mechanical stimuli, is associated with peripheral neuropathy and has been attributed to the central sprouting of A13 fibers (low threshold mechanoreceptors) into the superficial dorsal horn of the spinal cord, where they form functional synapses with nociceptive neurons that normally relay painful stimuli. We are interested in identifying the molecules and elucidating the mechanisms that enable axon sprouting and aberrant synapse formation.